期刊
ACTA NEUROLOGICA SCANDINAVICA
卷 122, 期 -, 页码 82-87出版社
WILEY
DOI: 10.1111/j.1600-0404.2010.01382.x
关键词
alpha-synuclein; parkin; proteasome; ubiquitin
Parkinson's disease (PD) is a primary neurodegenerative movement disorder. In most cases it occurs as a sporadic type of disease, but there are also rare familial forms. Pathologically Parkinson's disease is characterized by loss of dopaminergic neurons in the compact part of substantia nigra. As a part of the neurodegenerative process protein aggregates will accumulate as Lewy bodies in dopaminergic neurons (1). In addition, non-dopaminergic neurons are known to be affected in Parkinsons's disease, for example, in several brain stem nuclei and the olfactoric bulb (2-4). The pathogenic process underlying the death of dopaminergic neurons is far from fully understood. Along with mitochondrial dysfunction, excitotoxicity, neuroinflammation and oxidative stress (5-8), recent evidence indicates that accumulation of protein filaments in Lewy bodies actively takes part in the degeneration of neurons. This will be further discussed below.
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